Mismatch between BDNF mRNA and protein expression in the developing visual cortex: the role of visual experience

Abstract

Brain-derived neurotrophic factor (BDNF) messenger RNA (mRNA) expression in the rat visual cortex of young and postnatal day 90 (P90) animals is developmentally regulated and influenced by visual experience. In the present paper we compared the expression of BDNF mRNA to the actual changes of BDNF protein occurring during postnatal development and verified whether BDNF protein distribution is controlled by visual activity. To achieve this aim we analysed BDNF mRNA and/or BDNF protein cellular distribution in the rat visual cortex at different postnatal ages by using immunohistochemistry and highly sensitive in situ hybridization. We found that before eye opening (P13), in all cortical layers a large number of visual cortical neurons contain BDNF mRNA with no detectable amount of BDNF protein. At later ages (P23 and P90), the number of BDNF-immunostained cells increases; most neurons are double labelled for BDNF mRNA and protein, and a small group of neurons is labelled only for BDNF protein. The cellular increase of BDNF immunolabelling is blocked in animals deprived of visual experience from birth (dark rearing), with a large population of neurons containing BDNF mRNA but not BDNF protein. This is similar to what is observed before eye opening. Exposure of dark-reared rats to a brief period (2 h) of light restores a good match between BDNF mRNA and BDNF protein cellular expression. We propose that visual experience controls the neuronal content of BDNF mRNA and BDNF protein in developing visual cortex.

BDNF rs6265 methylation and genotype interact on risk for schizophrenia

“…This may raise the concern that BDNF rs6265 methylation represents something indirectly associated with schizophrenia, rather than a risk factor. However, since the expression of BDNF mRNA does not reflect the rate of protein synthesized, 42 the relationship of BDNF rs6265 methylation with BDNF protein level may also be the result of the contribution of other elements, such as the expression of non-coding transcripts, affecting the level of BDNF protein by acting at a post-transcriptional level. 43,44 Moreover, since human platelets represent a main source of serum BDNF protein but not of BDNF mRNA, serum BDNF has been postulated not to originate from megakaryocyte precursor cells, while potential sources include CNS 41,45,46 ; indeed, it has been shown that BDNF can readily cross the brain-blood barrier.…”

Pharmacological Profile of Brain-derived Neurotrophic Factor (BDNF) Splice Variant Translation Using a Novel Drug Screening Assay

“…Similarly, YAC or BAC transgenic mouse lines were used to monitor mRNA expression (14 -16). However, it is very well known that the levels of the mRNA encoding BDNF do not correspond to the actual BDNF protein levels in vivo (43).…”

“Let There be Light!” pigeon eggs are regularly exposed to light during breeding

“…These activity-dependent signalling pathways induce neural gene transcription by modulating the function of transcriptional activators and repressors which finally lead to structural changes of the nerve cells (West and Grace, 2002). Accordingly, 2-4 h of light stimulation are sufficient to increase dendritic growth rates (Sin et al, 2002), or to enhance translation of the neurotrophic factor BDNF (Tropea et al, 2001) while blocking synaptic activity for 1 h enhances tectal cell death (Galliresta et al, 1993) and reduces growth of tectal dendrites or promotes arborisation of retinal ganglion cell axons (O'Rourke et al, 1994;Rajan et al, 1999;Cohen-Cory, 1999). Increased axonal arbor dynamics are also achieved within 2 h by tectal BDNF application (Cohen-Cory and Fraser, 1995; Alsina et al, 2001).…”